Background: OPCML belongs to the IgLON family of Ig domain&ndash;containing GPI-anchored cell adhesion molecules and was recently found to be involved in carcinogenesis, while its role in gastric cancer remains unclear.

Methods: We assessed expression and biological behavior of OPCML in gastric cancer.

Results: OPCML expression was markedly reduced in tumor tissues and cancer cell lines. Decreased OPCML expression had a significant association with unfavorable tumor stage (p&nbsp;=&nbsp;0.007) and grading (p&nbsp;&lt;&nbsp;0.001). Furthermore, the results revealed that OPCML was an independent prognostic factor for overall survival in gastric cancer (p&nbsp;=&nbsp;0.002). In addition, ectopic expression of OPCML in cancer cells significantly inhibited cell viability (p&nbsp;&lt;&nbsp;0.01) and colony formation (p&nbsp;&lt;&nbsp;0.001), arrest cell cycle in G0/G1 phase and induced apoptosis, and suppressed tumor formation in nude mice. The alterations of phosphorylation status of AKT and its substrate GSK3&beta;, up-regulation of pro-apoptotic regulators including caspase-3, caspase-9 and PARP, and up-regulation of cell cycle regulator p27, were implicated in the biological activity of OPCML in cancer cells.

Conclusion: Down-regulated OPCML expression might serve as an independent predictor for unfavorable prognosis of patients, and the biological behavior supports its role as a tumor suppressor in gastric cancer.

Electronic supplementary material: The online version of this article (doi:10.1186/s12885-017-3203-y) contains supplementary material, which is available to authorized users.

Mentions:
To understand the function of OPCML gene in gastric cancer, we assessed the effect of ectopic expression of OPCML on the growth of SGC-7901 and BGC-823 cells in which OPCML gene was silenced. As shown by RT-PCR and western blot, OPCML was significantly over-expressed in SGC-7901 and BGC-823 cells after stably transfected with OPCML-pcDNA3.1 plasmid (Fig. 3a, b). Representative clones of SGC-7901 and BGC-823 transfectants were cultivated and assayed for their viability using CCK-8 assay. Ectopic expression of OPCML resulted in an approximately 36% (P < 0.01) and 42% (P < 0.01) decrease of cell viability in SGC-7901 and BGC-823 cells at the 5th day of experiment, respectively (Fig. 3c, d). Colony formation assay revealed that the number of colonies formed by OPCML transfectants were significantly fewer compared with empty vector transfectants. OPCML SGC-7901 and BGC-823 transfectants exhibited an approximately 54% (P < 0.001) and 65% (P < 0.001) reduction in colony formation respectively, in comparison to empty vector–transfected control cells (Fig. 3e, f). Soft agar assay further confirmed the significant suppressive effect of OPCML on the growth of SGC-7901 (P < 0.0001) and BGC-823 cells (P < 0.001) (Fig. 3g, h).Fig. 3

Mentions:
To understand the function of OPCML gene in gastric cancer, we assessed the effect of ectopic expression of OPCML on the growth of SGC-7901 and BGC-823 cells in which OPCML gene was silenced. As shown by RT-PCR and western blot, OPCML was significantly over-expressed in SGC-7901 and BGC-823 cells after stably transfected with OPCML-pcDNA3.1 plasmid (Fig. 3a, b). Representative clones of SGC-7901 and BGC-823 transfectants were cultivated and assayed for their viability using CCK-8 assay. Ectopic expression of OPCML resulted in an approximately 36% (P < 0.01) and 42% (P < 0.01) decrease of cell viability in SGC-7901 and BGC-823 cells at the 5th day of experiment, respectively (Fig. 3c, d). Colony formation assay revealed that the number of colonies formed by OPCML transfectants were significantly fewer compared with empty vector transfectants. OPCML SGC-7901 and BGC-823 transfectants exhibited an approximately 54% (P < 0.001) and 65% (P < 0.001) reduction in colony formation respectively, in comparison to empty vector–transfected control cells (Fig. 3e, f). Soft agar assay further confirmed the significant suppressive effect of OPCML on the growth of SGC-7901 (P < 0.0001) and BGC-823 cells (P < 0.001) (Fig. 3g, h).Fig. 3

Background: OPCML belongs to the IgLON family of Ig domain&ndash;containing GPI-anchored cell adhesion molecules and was recently found to be involved in carcinogenesis, while its role in gastric cancer remains unclear.

Methods: We assessed expression and biological behavior of OPCML in gastric cancer.

Results: OPCML expression was markedly reduced in tumor tissues and cancer cell lines. Decreased OPCML expression had a significant association with unfavorable tumor stage (p&nbsp;=&nbsp;0.007) and grading (p&nbsp;&lt;&nbsp;0.001). Furthermore, the results revealed that OPCML was an independent prognostic factor for overall survival in gastric cancer (p&nbsp;=&nbsp;0.002). In addition, ectopic expression of OPCML in cancer cells significantly inhibited cell viability (p&nbsp;&lt;&nbsp;0.01) and colony formation (p&nbsp;&lt;&nbsp;0.001), arrest cell cycle in G0/G1 phase and induced apoptosis, and suppressed tumor formation in nude mice. The alterations of phosphorylation status of AKT and its substrate GSK3&beta;, up-regulation of pro-apoptotic regulators including caspase-3, caspase-9 and PARP, and up-regulation of cell cycle regulator p27, were implicated in the biological activity of OPCML in cancer cells.

Conclusion: Down-regulated OPCML expression might serve as an independent predictor for unfavorable prognosis of patients, and the biological behavior supports its role as a tumor suppressor in gastric cancer.

Electronic supplementary material: The online version of this article (doi:10.1186/s12885-017-3203-y) contains supplementary material, which is available to authorized users.